Certain arenaviruses are the causative agents of several severe and frequently fatal human hemorrhagic fevers. Among these pathogens, Lassa fever virus (LFV) produces high morbidity and mortality throughout West Africa. There are an estimated 250,000 persons infected by LFV per year, of whom 5,000 die. Lymphocytic choriomeningitis virus (LCMV) another arenavirus, can also cause human diseases, but has been studies primarily as the prototype of arenaviruses and a classical model of viral immunology and pathogenesis. Arenaviruses can cause a persistent infection in their rodent hosts, and humans who come in contact with excreted arenaviruses may become infected.
An understanding of the early events of arenavirus-host cell interaction, the viruses' tropism and pathogenesis, should facilitate the development of the strategies to block initial virus-cell interactions. For initiation of infection, the LCMV glycoprotein GP-1 on the surface of the virion likely anchors the virus to the cell surface via a proteinaceous receptor(s). Since LCMV infects a wide variety of cell types from many different mammalian hosts both in vitro and in vivo, this receptor is likely conserved and ubiquitously expressed. However, LCMV attaches poorly to lymphoid cells or cells adapted to grow in suspension, suggesting that the receptor may be involved in adhesion interactions.
Previously, a virus overlay protein blot assay (VOPBA) revealed a single high molecular weight glycoprotein that specifically bound to purified LCMV (P. Borrow and M. Oldstone, J. Virol. 66: 7270 (1992)). This molecule was identified as a glycoprotein sensitive to a battery of proteases, glycosidases and tunicamycin (P. Borrow and M. Oldstone, J. Virol. 66: 7270 (1992)).